Sympathetic nervous system activity is an important independent determinant of energy expenditure. Furthermore, in Pima Indians, a population prone to increased adiposity and type 2 diabetes, sympathetic nervous system activity is lower compared to Caucasians, and within the Pima Indian population lower sympathetic nervous system activity, as measured by urine catecholamines predicts weight gain. [unreadable] [unreadable] Direct cannulation of the peroneal nerve provides a direct measurement of muscle sympathetic nerve activity. This technique was used to assess change in muscle sympathetic nervous system activity following a test meal, and to determine if sympathetic nervous system activity following a meal differed between Pima Indians and Caucasians. In addition, visual analogue scores to record hunger and satiety before and following the meal, and blood for glucose, insulin, and gut hormones (including GLP-1) were collected to determine the relationship of sympathetic nerve activity to these hormones.[unreadable] [unreadable] Using positron emission scanning and brain MRI, neuroanatomical correlates of hunger and satiety have been investigated. Importantly, recent analyses of this collected data has indicated that the left dorsolateral prefrontal cortex, and area of the brain important in reward processing, may be a satiety center. Neuronal activation following a meal is consistently lower in this area in obese versus lean individuals, in both men and women. Furthermore, in individuals who have lost weight, neuronal activation is closer to that of lean, and higher than in obese individuals. In subjects with Prader-Willi syndrome, a monogenic form of obesity characterized by extreme hyperphagia, neuronal activity following a meal actually decreases, and is significantly different compared to controls matched for adiposity. Post-prandial glucagons like-peptide-1 response is also positively associated with neuronal activity in this same brain region.